In contrast, two different, none KIT-dependent MC-deficient mouse models (Cpa3cre/+ (Cre recombinase in the carboxypeptidase A locus) and Mcpt5-Cre+ R-DTA+ (MC specific expression of diphtheria toxin A)) exhibited no phenotypic impact on the development of obesity or on its metabolic consequences, including insulin resistance, hepatic steatosis, or inflammation [9,10]. This evidence concerns the gene KIT and obesity due to melanocortin 4 receptor deficiency.